scholarly journals Temporal and spatial changes in reactive astrogliosis examined by 18F-THK5351 positron emission tomography in a patient with severe traumatic brain injury

2021 ◽  
Vol 5 (1) ◽  
Author(s):  
Tetsuhiro Hatakeyama ◽  
Kenya Kawakita ◽  
Nobuyuki Kawai ◽  
Hajime Shishido ◽  
Yuka Yamamoto ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Positron Emission Tomography ◽  
Brain Injury ◽  
Emission Tomography ◽  
Reactive Astrogliosis ◽  
Positron Emission ◽  
Spatial Changes ◽  
Severe Tbi ◽  
Temporal And Spatial ◽  
The Brain

Abstract Background The positron emission tomography (PET) radioligand 18F-THK5351 is now used to evaluate monoamine oxidase B expression in the reactive astrogliosis seen in various central nervous diseases. Traumatic brain injury (TBI) is known to induce reactive astrogliosis in the lesion site. This is a first report to examine the spatial and temporal changes in reactive astrogliosis as evaluated by 18F-THK5351 after a severe TBI. Case presentation A 27-year-old man suffering from a severe TBI with multiple brain contusions was examined using 18F-THK5351 PET/CT in the subacute and chronic phases after the injury. The first PET scan, performed 46 days after the TBI, showed intense uptake of 18F-THK5351 in and around the brain contusions. The second PET scan, performed 271 days after the TBI, showed reduced uptake of 18F-THK5351 at the original sites of the brain contusions and increased uptakes in the white matter surrounding the contusions and the corpus callosum. The patient exhibited sustained improvement of neuropsychological impairment between the two PET examinations and remarkable recovery from the severe TBI. Conclusions There were evident temporal and spatial changes in 18F-THK5351 uptake in the traumatized brain between the two PET examinations. These changes may have been related to the remarkable neurological recovery in this patient. The degree and distribution of reactive astrogliosis detected by 18F-THK5351 PET may be useful in assessing pathophysiology and predicting prognosis in TBI patients.

scholarly journals Traumatic brain injury induces elevation of Co in the human brain

Metallomics ◽  
2015 ◽  
Vol 7 (1) ◽  
pp. 66-70 ◽  
Author(s):  
Blaine R. Roberts ◽  
Dominic J. Hare ◽  
Catriona A. McLean ◽  
Alison Conquest ◽  
Monica Lind ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Positron Emission Tomography ◽  
Brain Injury ◽  
Human Brain ◽  
Injury Severity ◽  
Acute Brain Injury ◽  
Emission Tomography ◽  
Positron Emission ◽  
The Brain

Following acute brain injury (<3 hours post-event), cobalt levels in the brain are significantly elevated. This elevation may have important implications for positron emission tomography neuroimaging for assessing brain injury severity.

scholarly journals Metabolic Crisis without Brain Ischemia is Common after Traumatic Brain Injury: A Combined Microdialysis and Positron Emission Tomography Study

2005 ◽  
Vol 25 (6) ◽  
pp. 763-774 ◽  
Author(s):  
Paul Vespa ◽  
Marvin Bergsneider ◽  
Nayoa Hattori ◽  
Hsiao-Ming Wu ◽  
Sung-Cheng Huang ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Positron Emission Tomography ◽  
Brain Injury ◽  
Brain Ischemia ◽  
Emission Tomography ◽  
Cerebral Microdialysis ◽  
Energy Crisis ◽  
Metabolic Crisis ◽  
Positron Emission ◽  
Pyruvate Ratio

Brain trauma is accompanied by regional alterations of brain metabolism, reduction in metabolic rates and possible energy crisis. We hypothesize that microdialysis markers of energy crisis are present during the critical period of intensive care despite the absence of brain ischemia. In all, 19 brain injury patients (mean GCS 6) underwent combined positron emission tomography (PET) for metabolism of glucose (CMRglu) and oxygen (CMRO2) and cerebral microdialysis (MD) at a mean time of 36 h after injury. Microdialysis values were compared with the regional mean PET values adjacent to the probe. Longitudinal MD data revealed a 25% incidence rate of metabolic crisis (elevated lactate/pyruvate ratio (LPR)>40) but only a 2.4% incidence rate of ischemia. Positron emission tomography imaging revealed a 1% incidence of ischemia across all voxels as measured by oxygen extraction fraction (OEF) and cerebral venous oxygen content (CvO2). In the region of the MD probe, PET imaging revealed ischemia in a single patient despite increased LPR in other patients. Lactate/pyruvate ratio correlated negatively with CMRO2 ( P<0.001), but not with OEF or CvO2. Traumatic brain injury leads to a state of persistent metabolic crisis as reflected by abnormal cerebral microdialysis LPR that is not related to ischemia.

scholarly journals From positron emission tomography to cell analysis of the 18-kDa Translocator Protein in mild traumatic brain injury

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Clément Delage ◽  
Nicolas Vignal ◽  
Coralie Guerin ◽  
Toufik Taib ◽  
Clément Barboteau ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Positron Emission Tomography ◽  
Flow Cytometry ◽  
Microglial Activation ◽  
Translocator Protein ◽  
Emission Tomography ◽  
Flow Cytometry Analysis ◽  
Positron Emission ◽  
The Brain ◽  
Tspo Expression

AbstractTraumatic brain injury (TBI) leads to a deleterious neuroinflammation, originating from microglial activation. Monitoring microglial activation is an indispensable step to develop therapeutic strategies for TBI. In this study, we evaluated the use of the 18-kDa translocator protein (TSPO) in positron emission tomography (PET) and cellular analysis to monitor microglial activation in a mild TBI mouse model. TBI was induced on male Swiss mice. PET imaging analysis with [18F]FEPPA, a TSPO radiotracer, was performed at 1, 3 and 7 days post-TBI and flow cytometry analysis on brain at 1 and 3 days post-TBI. PET analysis showed no difference in TSPO expression between non-operated, sham-operated and TBI mice. Flow cytometry analysis demonstrated an increase in TSPO expression in ipsilateral brain 3 days post-TBI, especially in microglia, macrophages, lymphocytes and neutrophils. Moreover, microglia represent only 58.3% of TSPO+ cells in the brain. Our results raise the question of the use of TSPO radiotracer to monitor microglial activation after TBI. More broadly, flow cytometry results point the lack of specificity of TSPO for microglia and imply that microglia contribute to the overall increase in TSPO in the brain after TBI, but is not its only contributor.

scholarly journals Cobalt-55 positron emission tomography in traumatic brain injury: a pilot study.

1996 ◽  
Vol 60 (2) ◽  
pp. 221-224 ◽  
Author(s):  
H M Jansen ◽  
J van der Naalt ◽  
A H van Zomeren ◽  
A M Paans ◽  
L Veenma-van der Duin ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Positron Emission Tomography ◽  
Brain Injury ◽  
Pilot Study ◽  
Emission Tomography ◽  
Positron Emission
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